To date there has been poor translation of immunotherapies from rodent models to treatment of progressive multiple sclerosis (MS). In the robust, relapsing Biozzi ABH mouse model of MS, using a combination of a transient deletion of T cells followed by intravenous (i.v.) myelin antigen administration, established relapsing disease in EAE can be effectively silenced. However, when treatment was initiated in late stage chronic-relapsing disease, despite inhibition of further relapses, mice demonstrated evidence of disease progression shown by a deterioration in mobility and development of spasticity and indicates that targeting relapsing, immunological components of MS alone is unlikely to be sufficient to control progression in the late stages of MS.

Note this is real therapeutic treatment unlike 99% of other EAE studies and starts after animals have disease. If the same treatment is started after 3-4 attacks then number of subsequent attacks is 0% and n is greater than 100 but too late and progression occurs. SCH= spinal cord homogenate Ag= antigen d= depleting

Relapsing EAE can be switched off within 24 hours at any stage of the disease using a combination of transient T cell depletion and antigen-specific tolerance. However, the problem is if there is too much damage, secondary progression kicks in which is no longer responds to the same treatment. The inference is be early and aggressive in treatment and you may stop MS in its tracks. This is an antigen-specific treatment and so does not stop immune response to infections...How is this translated to MS?